Search results for " Knockout"

showing 10 items of 764 documents

The Bile Acid Receptor GPBAR-1 (TGR5) Modulates Integrity of Intestinal Barrier and Immune Response to Experimental Colitis

2011

Background GP-BAR1, a member G protein coupled receptor superfamily, is a cell surface bile acid-activated receptor highly expressed in the ileum and colon. In monocytes, ligation of GP-BAR1 by secondary bile acids results in a cAMP-dependent attenuation of cytokine generation. Aims To investigate the role GP-BAR1 in regulating intestinal homeostasis and inflammation-driven immune dysfunction in rodent models of colitis. Methods Colitis was induced in wild type and GP-BAR1−/− mice by DSS and TNBS administration. Potential GP-BAR1 agonists were identified by in silico screening and computational docking studies. Results GP-BAR1−/− mice develop an abnormal morphology of colonic mucous cells a…

Cholera ToxinCD14Biophysicslcsh:MedicineInflammationGastroenterology and HepatologyBiologyLigandsBiochemistryPermeabilityReceptors G-Protein-CoupledTight JunctionsMiceCrohn DiseaseCiprofloxacinMolecular Cell BiologymedicineAnimalsUlcerative ColitisIntestinal MucosaProtein PrecursorsBiomacromolecule-Ligand InteractionsColitislcsh:ScienceReceptorBiologyMice KnockoutMultidisciplinaryIntestinal permeabilityHaptoglobinsPhysicsInflammatory Bowel Diseaselcsh:RImmunityZonulinColitisFlow Cytometrymedicine.diseaseMolecular biologyG protein-coupled bile acid receptorImmunologyTLR4Medicinelcsh:Qmedicine.symptomCytometryResearch ArticlePLoS ONE
researchProduct

EphrinB2 controls vessel pruning through STAT1-JNK3 signalling

2014

Angiogenesis produces primitive vascular networks that need pruning to yield hierarchically organized and functional vessels. Despite the critical importance of vessel pruning to vessel patterning and function, the mechanisms regulating this process are not clear. Here we show that EphrinB2, a well-known player in angiogenesis, is an essential regulator of endothelial cell death and vessel pruning. This regulation depends upon phosphotyrosine-EphrinB2 signalling repressing c-jun N-terminal kinase 3 activity via STAT1. JNK3 activation causes endothelial cell death. In the absence of JNK3, hyaloid vessel physiological pruning is impaired, associated with abnormal persistence of hyaloid vessel…

Chromatin ImmunoprecipitationCell SurvivalAngiogenesisImmunoblottingRegulatorFluorescent Antibody TechniqueNeovascularization PhysiologicGeneral Physics and AstronomyEphrin-B2Persistent Hyperplastic Primary VitreousIn Vitro TechniquesBiologyBioinformaticsMicrophthalmiaArticleGeneral Biochemistry Genetics and Molecular BiologyNeovascularizationMiceMitogen-Activated Protein Kinase 10Human Umbilical Vein Endothelial CellsmedicineAnimalsHumansImmunoprecipitationInvolution (medicine)Pruning (decision trees)Cell ProliferationMice KnockoutMultidisciplinaryNeovascularization PathologicfungiEndothelial CellsRetinal VesselsGeneral ChemistryFlow Cytometrymedicine.diseaseCell biologyEndothelial stem cellSTAT1 Transcription Factornervous systemPersistent hyperplastic primary vitreousGene Knockdown Techniquescardiovascular systemmedicine.symptomSignal TransductionNature Communications
researchProduct

In vitro P-glycoprotein efflux inhibition by atypical antipsychotics is in vivo nicely reflected by pharmacodynamic but less by pharmacokinetic chang…

2011

Abstract Background P-glycoprotein (P-gp), an efflux transporter of the blood–brain barrier, limits the access of multiple xenobiotics to the central nervous system (CNS). Thus drug-dependent inhibition, induction or genetic variation of P-gp impacts drug therapy. Methods We investigated atypical antipsychotics and their interaction with P-gp. Amisulpride, clozapine, N-desmethylclozapine, olanzapine, and quetiapine were assessed in vitro on their inhibitory potential and in vivo on their disposition in mouse serum and brain, and behaviourally on the RotaRod test. In vivo wildtype (WT) and mdr1a/1b double knockout mice (mdr1a/1b (−/−, −/−); KO) were investigated. Results In rhodamine 123 eff…

Clinical BiochemistryIn Vitro TechniquesPharmacologyToxicologyBlood–brain barrierBiochemistryRhodamine 123Rotarod performance testMiceBehavioral Neurosciencechemistry.chemical_compoundPharmacokineticsIn vivoCell Line TumormedicineAnimalsRhodamine 123ATP Binding Cassette Transporter Subfamily B Member 1Biological PsychiatryClozapineP-glycoproteinMice KnockoutPharmacologybiologyReceptors Dopamine D2Protein Transportmedicine.anatomical_structurechemistryRotarod Performance Testbiology.proteinDopamine AntagonistsEffluxAntipsychotic Agentsmedicine.drugPharmacology Biochemistry and Behavior
researchProduct

Ikaros-1 couples cell cycle arrest of late striatal precursors with neurogenesis of enkephalinergic neurons

2010

et al.

Cyclin-Dependent Kinase Inhibitor p21CalbindinsEnkephalinNeurogenesiseducationCentral nervous systemCell Cycle ProteinsStriatumSubstance PBiologyEfferent PathwaysCalbindinIkaros Transcription FactorMiceS100 Calcium Binding Protein GmedicineAnimalsProgenitor cellTranscription factorhealth care economics and organizationsHomeodomain ProteinsMice KnockoutNeuronsStem CellsGeneral NeuroscienceNeurogenesisCell DifferentiationEnkephalinsCell cycleCorpus StriatumGenes cdcMice Inbred C57BLmedicine.anatomical_structurenervous systemTrans-ActivatorsNeuroscienceTranscription FactorsThe Journal of Comparative Neurology
researchProduct

Transcriptional repression of Bmp2 by p21(Waf1/Cip1) links quiescence to neural stem cell maintenance.

2013

Relative quiescence and self renewal are defining features of adult stem cells, but their potential coordination remains unclear. Subependymal neural stem cells (NSCs) lacking cyclin-dependent kinase (CDK) inhibitor (CKI) 1a (p21) exhibit rapid expansion that is followed by their permanent loss later in life. Here we demonstrate that transcription of the gene encoding bone morphogenetic protein 2 (Bmp2) in NSCs is under the direct negative control of p21 through actions that are independent of CDK. Loss of p21 in NSCs results in increased levels of secreted BMP2, which induce premature terminal differentiation of multipotent NSCs into mature non-neurogenic astrocytes in an autocrine and/or …

Cyclin-Dependent Kinase Inhibitor p21Time FactorsCellular differentiationBone Morphogenetic Protein 2Nerve Tissue ProteinsBiologyTransfectionParacrine signallingMiceNeural Stem CellsCyclin-dependent kinaseTransduction GeneticSubependymal zoneAnimalsCell Line TransformedRegulation of gene expressionMice KnockoutGeneral NeuroscienceNeurogenesisCell CycleAge FactorsCell DifferentiationNeural stem cellCell biologyKi-67 AntigenBromodeoxyuridineGene Expression RegulationMutagenesisCulture Media Conditionedbiology.proteinNeoplastic Stem CellsCarrier ProteinsNeuroscienceAdult stem cellSubcellular FractionsNature neuroscience
researchProduct

Cutting edge: priming of CTL by transcutaneous peptide immunization with imiquimod.

2005

Abstract CTL are important in combating cancer and viruses. Therefore, triggering the complete potential of CTL effector functions by new vaccination strategies will not only improve prophylaxis of tumor or virus-related diseases, but also open opportunities for effective therapeutic immunizations. Using transcutaneous immunization, we show that epicutaneous (e.c.)4 application of an ointment containing a CTL epitope and the TLR7 ligand imiquimod is highly effective in activating T cells in mice using TCR-transgenic CTL or in wild-type mice. Transcutaneous immunization-activated CTL mount a full-blown immune response against the target epitope characterized by proliferation, cytolytic activ…

Cytotoxicity ImmunologicAdoptive cell transferImmunologyReceptors Antigen T-CellPriming (immunology)Epitopes T-Lymphocytechemical and pharmacologic phenomenaImiquimodMice TransgenicAdministration CutaneousLymphocyte ActivationResting Phase Cell CycleEpitopeMiceImmune systemmedicineImmunology and AllergyAnimalsCells CulturedMice KnockoutImiquimodbusiness.industryTLR7VirologyAdoptive TransferVaccinationMice Inbred C57BLCTL*Protein TransportImmunologyVaccines SubunitAminoquinolinesLymph NodesbusinessSpleenmedicine.drugT-Lymphocytes CytotoxicJournal of immunology (Baltimore, Md. : 1950)
researchProduct

Immunosurveillance of lung melanoma metastasis in EBI-3-deficient mice mediated by CD8+ T cells.

2008

Abstract EBV-induced gene 3 (EBI-3) codes for a soluble type I receptor homologous to the p40 subunit of IL-12 that is expressed by APCs following activation. In this study, we assessed the role of EBI-3 in a model of lung melanoma metastasis. Intravenous injection of the B16-F10 cell line resulted in a significant reduction of lung tumor metastasis in EBI-3−/− recipient mice compared with wild-type mice. The immunological finding accompanying this effect was the expansion of a newly described cell subset called IFN-γ producing killer dendritic cells associated with CD8+ T cell responses in the lung of EBI-3−/− mice including IFN-γ release and TNF-α-induced programmed tumor cell death. Depl…

Cytotoxicity ImmunologicAdoptive cell transferLung NeoplasmsT cellImmunologyMelanoma ExperimentalBiologyCD8-Positive T-LymphocytesArticleMetastasisMinor Histocompatibility AntigensGene Knockout TechniquesMiceCell Line TumormedicineImmunology and AllergyCytotoxic T cellAnimalsLung MelanomaReceptors CytokineImmunologic SurveillanceCell Line TransformedMice KnockoutMelanomamedicine.diseaseImmunosurveillanceMice Inbred C57BLmedicine.anatomical_structureCell Transformation NeoplasticImmunologyInjections IntravenousAnimals; CD8-Positive T-Lymphocytes; Cell Line Transformed; Cell Line Tumor; Cell Transformation Neoplastic; Cytotoxicity Immunologic; Gene Knockout Techniques; Immunologic Surveillance; Injections Intravenous; Lung Neoplasms; Melanoma Experimental; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasm Transplantation; Receptors Cytokine; T-Box Domain ProteinsCancer researchT-Box Domain ProteinsCD8Neoplasm Transplantation
researchProduct

Type I Interferon Protects Antiviral CD8+ T Cells from NK Cell Cytotoxicity

2014

Summary Despite development of new antiviral drugs, viral infections are still a major health problem. The most potent antiviral defense mechanism is the innate production of type I interferon (IFN-I), which not only limits virus replication but also promotes antiviral T cell immunity through mechanisms, which remain insufficiently studied. Using the murine lymphocytic choriomeningitis virus model system, we show here that IFN-I signaling on T cells prevented their rapid elimination in vivo. Microarray analyses uncovered that IFN-I triggered the expression of selected inhibitory NK-cell-receptor ligands. Consequently, T cell immunity of IFN-I receptor (IFNAR)-deficient T cells could be rest…

Cytotoxicity ImmunologicImmunologyMedizinReceptor Interferon alpha-betaCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisVirus ReplicationLymphocytic choriomeningitisVirusMiceImmunityInterferonmedicineAnimalsLymphocytic choriomeningitis virusImmunology and AllergyCytotoxic T cellCells CulturedMice KnockoutbiologyPerforinNFIL3medicine.diseaseVirologyImmunity InnateKiller Cells NaturalMice Inbred C57BLBasic-Leucine Zipper Transcription FactorsInfectious DiseasesViral replicationPerforinInterferon Type IImmunologybiology.proteinSignal Transductionmedicine.drugImmunity
researchProduct

Poly(ADP-ribosyl)ation accelerates DNA repair in a pathway dependent on Cockayne syndrome B protein

2003

Activation of poly(ADP-ribose)polymerases 1 and 2 (PARP-1 and PARP-2) is one of the earliest responses of mammalian cells to DNA damage by numerous genotoxic agents. We have analysed the influence of PARP inhibition, either achieved by over-expression of the DNA binding domain of PARP-1 or by treatment with 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone, on the repair of single-strand breaks (SSB), pyrimidine dimers and oxidative base modifications sensitive to Fpg protein (mostly 8-hydroxyguanine) in mammalian cells at very low, non-cytotoxic levels of DNA damage. The data show that the repair rates of all three types of DNA damage are significantly lower in PARP-inhibited c…

DNA RepairDNA damageDNA repairPoly ADP ribose polymerase[SDV]Life Sciences [q-bio]Pyrimidine dimerBiologyPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorCockayne syndromeDexamethasone03 medical and health sciencesMice0302 clinical medicinePiperidinesCricetinaeGeneticsmedicineAnimalsPoly-ADP-Ribose Binding ProteinsComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Line TransformedMice Knockout0303 health sciencesDNA HelicasesArticlesDNADNA repair protein XRCC4Fibroblastsmedicine.diseaseIsoquinolinesMolecular biology3. Good healthDNA Repair Enzymes030220 oncology & carcinogenesisPoly(ADP-ribose) PolymerasesNucleotide excision repairDNA DamageSignal Transduction
researchProduct

Lentiviral-Mediated Gene Therapy in Fanconi Anemia-A Mice Reveals Long-Term Engraftment and Continuous Turnover of Corrected HSCs

2015

International audience; Fanconi anemia is a DNA repair-deficiency syndrome mainly characterized by cancer predisposition and bone marrow failure. Trying to restore the hematopoietic function in these patients, lentiviral vector-mediated gene therapy trials have recently been proposed. However, because no insertional oncogenesis studies have been conducted so far in DNA repair-deficiency syndromes such as Fanconi anemia, we have carried out a genome-wide screening of lentiviral insertion sites after the gene correction of Fanca-/- hematopoietic stem cells (HSCs), using LAM-PCR and 454-pyrosequencing. Our studies first demonstrated that transduction of Fanca-/- HSCs with a lentiviral vector d…

DNA RepairDNA repair[SDV]Life Sciences [q-bio]Genetic enhancementGenetic VectorsBiologymedicine.disease_causePolymerase Chain ReactionViral vectorCell LineMiceFanconi anemiaTransduction Genetichemic and lymphatic diseasesDrug DiscoveryGeneticsmedicineAnimalsMolecular BiologyGenetics (clinical)Mice KnockoutFanconi Anemia Complementation Group A ProteinLentivirusBone marrow failureGenetic Therapymedicine.diseaseHematopoietic Stem CellsFANCA3. Good health[SDV] Life Sciences [q-bio]Fanconi AnemiaCancer researchMolecular MedicineStem cellCarcinogenesis
researchProduct